Hemolytic uremic syndrome (HUS) is characterized by acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia. HUS occurs as a complication of childhood associated Streptococcus pneumoniae infections such as pneumonia, otitis media, and meningitis. Without proper diagnosis and treatment the outcome to HUS is almost always fatal. The bacterial factor leading to HUS has been identified as the pneumococcal neuraminidase, which exposes the Thomsen-Friedenreich antigen (T-antigen) on the surface of endothelial cells and red blood cells. The disease state occurs when antibodies to the T-antigen are present in infected individuals. My studies focus on describing the events that occur between the initial clinical presentation and the onset of HUS. I am working to mimic HUS in an animal model. I have been able to demonstrate exposure of T-antigen on kidneys and red blood cells during S. pneumoniae infection in mice. Future studies will examine the effect that localized kidney infection could contribute to the development of HUS. These studies will help physicians predict which S. pneumoniae infections will progress to become HUS and avoid practices that exacerbate HUS. [unreadable] [unreadable]